fosB Gene Products Trigger Cell Proliferation and Morphological Alteration with an Increased Expression of a Novel Processed Form of Galectin-1 in the Rat 3Y1 Embroyo Cell Line

Author:

Nishioka Tomoko12,Sakumi Kunihiko1,Miura Tomofumi1,Tahara Kazuki1,Horie Hidenori3,Kadoya Toshihiko4,Nakabeppu Yusaku1

Affiliation:

1. Division of Neurofunctional Genomics, Medical Institute of Bioregulation, Kyushu University, and CREST, Japan Science and Technology Corporation  3-1-1 Maidashi, Higashi-ku, Fukuoka 812–8582

2. Department of Obstetrics and Gynecology, School of Medicine, Fukuoka University  Fukuoka 814-0180

3. Advanced Research Center for Biological Science, Waseda University  2-7-5 Higashifushimi, Nishitokyo City, Tokyo 202-0021

4. Pharmaceutical Research Laboratory, Kirin Brewery Co. Ltd.  Takasaki 370-1295

Abstract

Abstract In this study, we established rat 3Y1 embryo cell lines expressing FosB and AFosB as fusion proteins (ER-FosB, ER-AFosB) with the ligand-binding domain of human estrogen receptor (ER). The binding of estrogen to the fusion proteins resulted in their nuclear translocation. After estrogen administration, exponentially growing cells expressing ER-AFosB, and to a lesser extent ER-FosB, underwent morphological alteration from the flat fibroblastic shape to an extended bipolar shape, and ceased proliferating. Such morphological alteration was also induced in quiescent cells expressing ER-AFosB and ER-FosB after one round of cell division triggered by estrogen administration. The cells expressing ER-AFosB changed shape frequently, and the content of F-actin in the cytoplasm detected by binding of Alexa 488-phalloidin significantly decreased after the morphological alteration. By two-dimensional gel electrophoresis analysis of cellular proteins from the cells expressing ER-AFosB, we identified several proteins whose expression either increased or decreased after estrogen administration. Two of these proteins were identified from their amino acid sequences as novel processed form of galectin-1.

Publisher

Oxford University Press (OUP)

Subject

Molecular Biology,Biochemistry,General Medicine

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